| First Author | Brown CR | Year | 1999 |
| Journal | J Infect Dis | Volume | 179 |
| Issue | 6 | Pages | 1573-6 |
| PubMed ID | 10228086 | Mgi Jnum | J:55169 |
| Mgi Id | MGI:1337436 | Doi | 10.1086/314774 |
| Citation | Brown CR, et al. (1999) Development of lyme arthritis in mice deficient in inducible nitric oxide synthase. J Infect Dis 179(6):1573-6 |
| abstractText | Nitric oxide (NO) is a powerful antimicrobial agent and an important regulatory molecule of the innate immune response. To determine if NO has a role in experimental Lyme disease, arthritis-resistant DBA/2J and arthritis- susceptible C3H/HeJ mice were bred to be genetically deficient for inducible NO synthase (iNOS), Following footpad injection of Borrelia burgdorferi, arthritis was similar between iNOS-deficient and control animals regardless of their genetic background. Histologic examination and arthritis severity scores of ankles revealed no differences in arthritis development between iNOS-deficient and control animals. Despite being deficient in a key antimicrobial agent, iNOS-deficient mice had tissue levels of B. Burgdorferi similar to those in control mice. Thus, NO does not have a critical role in susceptibility to Lyme arthritis through tissue damage via an overexuberant inflammatory response, nor is it required in resistance through the clearance of spirochetes from tissues. |
